Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005684 (bladder cancer)
 16,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Presentation of clinico-pathological correlation in a series of patients with bladder carcinoma. All of them had a complete pathological and clinical staging following TNM guidelines (UICC 1987). Clinical evaluation consisted of a clinical examination, urography and/or ultrasound, cystoscopy, bimanual palpation under anaesthesia and biopsy. As an option, pelvic CAT, MRI and a bone scan were performed. In all cases a reliable pathological staging was obtained, either from cystectomy or complete TUR. Overall, there is a 66% clinico-pathological correlation (60% for Ta category, 78% for T1, 25% for T2, 57% for T3, and 74% for T4). There is a global error of 34% (40% of cases clinically considered Ta were invasive, 16% T1 were pT2 or more, 42% T2 were pT3 or more, and 10% T3 were pT4; while 6% of those considered T1 were pTa, 33% of T2 were pTa or pT1, 33% of T3 were pT2 or less, and 26% of T4 were pT3 or less). We therefore conclude that when T is lower the risk of being clinically understaged is greater, while higher T values increase the risk of clinical overstaging. From a practical point of view, the most severe errors are in the understaging of T2 and T3 (pT3-pT4) tumours and the overstaging of T2 (pT1) tumours. When cystectomy is performed, the risk of understaging is greater for tumours interpreted as T2-T3 while the risk of overstaging T4 tumours is lower. We conclude that, even when adequate staging of bladder cancer is attempted, pre-treatment tumour classification using the diagnostic methods currently available is far from satisfactory.
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PMID:[Staging error in bladder carcinoma: anatomo-clinical correlation]. 771 56

Although the occurrence of bladder cancer is common, the molecular events underlying the pathogenesis of this cancer remain ill-defined. A loss of heterozygosity (LOH) at specific chromosomal loci may predispose individuals to the development of bladder cancer but this has not been examined in detail. Furthermore, the role that deletion or inactivation of putative tumour suppressor genes might play in the genesis of bladder cancer has not been established. In this study, allelic deletion analysis on the short arm of chromosome 17 of patients with primary bladder tumours failed to show deletion at 17p13 (0/7), a region known to contain the p53 tumour suppressor gene. Chromosome 11p15 showed allelic deletion at the IGF2 locus (2/7: 29%) and the PTH locus (1/11: 9%). However, no deletion was observed at the CALCA locus (0/6). LOH at 11p13, a region containing the Wilm's tumour suppressor gene (WT1), was also studied. Analysis of LOH at 11p13 showed deletion at the CAT locus (13/18: 72%), the delta J/D11S414 locus (5/15: 33%), the WT1 locus (7/14: 50%) and the FSHB locus (6/16: 38%). The significance of these findings is discussed.
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PMID:Loss of heterozygosity on chromosome 11p13 in primary bladder carcinoma. 810 Feb 10

It is well known that the expression level of the ICAM-1 and MHC is frequently altered in accordance with tumor progression, and the expression of oncogenes is significantly related to tumorigenesis, tumor progression, and/or metastatic potential. In this study, to investigate the relationship between the alteration in ICAM-1 and MHC expression with the tumor grade and/or cell differentiation, we examined the expression of ICAM-1 and HLA-DR before and after treatment with IFN-gamma in 4 human bladder cancer cell lines. We also analyzed the expression of c-Ha-ras and c-myc. Using flow cytometry, highly constitutive expression of ICAM-1 was detected in all cell lines tested except RT4 (grade I, well-differentiated, superficial). IFN-gamma was found to somewhat induce the expression of ICAM-1 in all cell lines except RT4. The constitutive expression of HLA-DR was not detected in any of the cell lines tested by flow cytometry and Northern blot. HLA-DR expression was induced by IFN-gamma in RT4 and J82 (grade III, anaplastic, invasive). Codon 12 point mutation of c-Ha-ras (GGC-->GTC; Gly-->Val) was detected in T24 (grade III, epidermoid, superficial) through single-strand conformation polymorphism, and sequencing analysis. Another point mutation at codon 27 was detected in TCCSUP (grade IV, distant metastatic), but this mutation was found to be silent (CAT-->CAC; His). Expression of c-myc was detected in J82 and TCCSUP by Northern blot. These findings, along with the clinical and pathological characteristics of the patients from whom the cell lines were established, might suggest that the expression of ICAM-1 seems to be associated with cell differentiation, and the inducibility of HLA-DR by IFN-gamma seems to be associated with the degree of malignancy. Expression of c-myc seems to be associated with invasiveness. However, a significant correlation between c-Ha-ras activation and tumor grade could not be observed.
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PMID:Induction of ICAM-1, HLA-DR molecules by IFN-gamma and oncogene expression in human bladder cancer cell lines. 939 53

We have previously shown that the DNA topoisomerase II alpha (topo II alpha) gene is down-regulated in VP16/VM26-resistant cells at the transcriptional level. To determine the DNA elements responsible for down-regulation, the transcriptional activities of luciferase reporter constructs containing various lengths of the promoter sequences were investigated by transient transfection of two resistant cell lines, KB/VP2 and KB/VM4. The transcriptional activities of the full-length promoter (-295 to +85) and of three deletion constructs (-197, -154 and -74 to +85) were significantly down-regulated in resistant cells. In contrast, the transcriptional activity of the minimal promoter (-20 to +85) in resistant cells was similar to that in parental KB cells. Furthermore, introduction of a mutation in ICE1 abolished the down-regulation of the topo II alpha promoter activity in drug-resistant cells. In vivo footprinting analysis of topo II alpha gene promoter revealed several specific protein-binding sites, a GC box, ICE1, ICE2 and ICE3. In vivo footprinting analysis also identified a cluster of hypersensitive sites. However, there was no marked difference in protein-binding sites between parental and resistant cells. To confirm our previous results, we have established the VP16-resistant cell lines T12-VP1 and T12-VP2 from T12 cells derived from human bladder cancer T24 cells stably transfected with the chloramphenicol acetyltransferase reporter gene driven by the topo II alpha gene promoter. The expression to topo II alpha was down-regulated in both cell lines. We also found that CAT gene expression was significantly decreased to one-fifth of that in T12 parental cells. These results suggest that the expression of the topo II alpha gene requires the binding of multiple factors to the core promoter and is down-regulated at the transcriptional level, probably through binding of a negative factor to ICE1 in drug-resistant cells.
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PMID:Structural and functional analysis of the control region of the human DNA topoisomerase II alpha gene in drug-resistant cells. 1040 35

Bladder cancer is a common neoplasm worldwide, consisting mainly of transitional cell carcinomas, while squamous, adenocarcinoma, and sarcomatoid bladder cancers account for the remaining cases. In the present study, multiplex fluorescence in situ hybridization (M-FISH) has been used to characterize chromosome rearrangements in eight transitional and one squamous cell carcinoma cell line, RT112, of UMUC-3, 5637, CAT(wil), FGEN, EJ28, J82, 253J, and SCaBER. Alterations of chromosome 9 are the most frequent cytogenetic and molecular findings in transitional cell carcinomas of all grades and stages, while changes of chromosomes 3, 4, 8, 9, 11, 14, and 17 are also frequently observed. In the present study, alterations previously described, including del(8)(p10), del(9)(p10), del(17)(p10), and overrepresentation of chromosome 20, as well as several novel findings, were observed. These novel findings were a del(15)(q15) and isochromosome 14q, both occurring in three of nine cell lines examined. These abnormalities may reflect changes in bladder tumor biology. M-FISH represents an effective preliminary screening tool for the characterization of complex tumor karyotypes.
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PMID:Novel chromosome findings in bladder cancer cell lines detected with multiplex fluorescence in situ hybridization. 1212 98

Oxidative damage induced by the generation of reactive oxygen species (ROS) is thought to be related to human cancer aetiology. Oxidative stress can result in DNA damage, including oxidized bases, formation of DNA adducts and DNA strand breaks, as well as lipid peroxidation, protein modification, membrane disruption and mitochondrial damage. The effect of reactive oxygen species is balanced by the antioxidant action ofnonenzymatic antioxidants (e.g. vitamins A, C, E, glutathione and flavonoids), as well as antioxidant enzymes. There are three main types of antioxidant defence enzymes: superoxide dismutases, catalase and glutathione peroxidases. A variety of cancer cells are known to have lower antioxidant enzyme activity when compared with their normal counterparts. Many studies have examined genetic variation in the genes coding for these enzymes and their relationship to cancer risk. Only a few genetic variants (single nucleotide polymorphisms--SNPs) in genes related to antioxidant defence were found to be associated with breast, prostate, lung, pancreatic, colorectal and bladder cancer. However, the results from these have been contradictory. Moreover, it is believed that environmental as well as genetic factors are implicated in the development of cancers, and consequently it is important to assess both genetic (including gene-gene association) and non-genetic (e.g. diet, supplementation, smoking and alcohol consumption) variability in the activities of defence enzymes in relation to cancer. In this review we focus on the biological function of antioxidant defence enzymes, and relationship between well-known SNPs in SOD1, SOD2, CAT, GPX1 and GPX4 genes and genetic susceptibility to cancer.
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PMID:[Polymorphisms in the oxidative stress-related genes and cancer risk]. 2502 46

Sonodynamic therapy (SDT) is a noninvasive ultrasound-triggered therapeutic strategy for site-specific treatment of tumors with great depth penetration. The design of nano-sonosensitizers suitable for SDT treatment of bladder cancer (BCa) post-intravesical instillation has not yet been reported. Herein, a transmucosal oxygen-self-production SDT nanoplatform is developed to achieve highly efficient SDT against BCa. In this system, fluorinated chitosan (FCS) is synthesized as a highly effective nontoxic transmucosal delivery carrier to assemble with meso-tetra(4-carboxyphenyl)porphine-conjugated catalase (CAT-TCPP). The formed CAT-TCPP/FCS nanoparticles after intravesical instillation into the bladder cavity exhibit excellent transmucosal and intratumoral penetration capacities and could efficiently relieve hypoxia in tumor tissues by the catalase-catalyzed O2 generation from tumor endogenous H2O2 to further improve the therapeutic efficacy of SDT to ablate orthotopic bladder tumors under ultrasound. Our work presents a nano-sonosensitizer formulation with FCS to enhance transmucosal delivery and intratumoral diffusion and CAT to improve tumor oxygenation, promising for instillation-based SDT to treat bladder tumors without the concern of systemic toxicity.
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PMID:Fluorinated Chitosan To Enhance Transmucosal Delivery of Sonosensitizer-Conjugated Catalase for Sonodynamic Bladder Cancer Treatment Post-intravesical Instillation. 3201 60